The chief purpose of the project is to understand adolescent sleep patterns as a function of underlying bioregulatory processes and their pubertal development. A common adolescent pattern is delayed and insufficient sleep, reflecting complex biopsychosocial interactions. The importance of this research stems from the known behavioral risk of insufficient sleep, including excessive daytime sleepiness, poor school performance, depressed mood, injuries and accidents. Using techniques of circadian rhythms and sleep research, the project undertakes three studies, each focusing on basic sleep regulatory issues. In Study 1, markers of the output of the endogenous circadian oscillator are measured in 108 girls and boys ages 10 to 14 years spanning pubertal stages. Sleep, mood, performance, sleepiness, deep body temperature (DBT), and urinary 6-sulphatoxymelatonin (6-SM) are measured during a weekend study. After sleeping in the laboratory on 2 nights, children remain awake in bed in a semi-recumbent position for 36 hours during a "constant routine" of lighting, food and fluid intake, and restricted activity. A recovery night follows. Circadian rhythm parameters include endogenous circadian phase (ECP) and amplitude of DBT, as well as times of 6-SM onset, offset, and peak. Recovery sleep variables mark homeostatic processes. Specific hypotheses are (1) circadian rhythms phase delay and (2) intensity of homeostatic sleep/wake mechanisms declines at puberty. This study also obtains a unique developmental data base of circadian rhythm and sleep variables across puberty. In Study 2, 60 girls and boys are evaluated in a 24-day laboratory "forced desynchrony" protocol from which the intrinsic period of the endogenous circadian oscillator can be accurately estimated. Measures are as in Study 1. After 2 baseline laboratory, days and before 2 recovery days, sleep/wake are scheduled on a 28-hour-day to which the endogenous circadian cannot entrain, thus freeing the endogenous rhythm from usual masking effects of sleep and wake. Constant routine assessment of ECP and ECA are made serially on three occasions when the trough of body temperature is out of phase with the scheduled sleep episode. This study tests the hypothesis that the period of the endogenous circadian oscillator lengthens at puberty; it also provides a rich body of information regarding sleep, wake, and circadian processes during pubertal maturation. Study 3 is a longitudinal study of the output of the endogenous circadian pacemaker in 32 normal children and 40 children at risk to develop depression by virtue of a family history of major depressive disorder. The constant routine paradigm Of Study 1 is used to measure ECP and ECA in normal and at-risk children at early and late stages of puberty. This study tests the hypothesis that ECP is more variable in the at-risk group and that extreme groups may show different sleep abnormalities. These findings may clarify the relationships of sleep, circadian rhythms, and mood disorder in adolescents.